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In utero and postnatal effects of sidestream cigarette smoke exposure on lung function, hyperresponsiveness, and neuroendocrine cells in rats.

A study was conducted to determine whether in-utero and/or postnatal exposure to sidestream smoke (SS) induced airway obstruction and hyperresponsiveness, and whether this effect was linked with neuroendocrine cell hyperplasia. Pregnant Sprague-Dawley-rats were exposed either to filtered air (FA) or SS containing a total suspended particulate concentration of 1.00mg/m3; a carbon-monoxide (630080) concentration of 4.9 parts per million; and a nicotine (54115) concentration of 344 micrograms/cubic meter. The exposure regimen lasted for 4 hours/day, 7 days/week from gestation day three until birth. Female pups were randomly assigned to litters. Some rats were exposed to FA or SS until 7 to 10 weeks of age, resulting in a total of four in-utero/postnatal exposure conditions: FA/FA, FA/SS, SS/FA, and SS/SS. The rats were killed, followed by removal of the lungs, which were in a buffer perfused system where measurements were made of dynamic compliance (Cdyn), lung resistance (RL), pulmonary artery pressure (Ppa), and methacholine reactivity. SS/SS exposure resulted in a 24% lower Cdyn and 6% lower RL compared with FA exposure, as well as a hyperreactivity to methacholine; the RL was increased to more than twofold that of FA/FA exposed lungs. SS/FA or FA/SS exposure did not change Cdyn or RL, or result in methacholine hyperreactivity. Ppa was not changed by SS. Neuroendocrine cells were identified with antibodies to neuron specific enolase and serotonin. More neuroendocrine cells were found in SS/FA or FA/SS exposed lungs compared with FA/FA lungs. A nonsignificant trend was seen for SS/FA or FA/SS rat lungs to have increased numbers of neuroendocrine cells. The authors conclude that SS/SS reduced lung compliance, increased lung hyperreactivity, and increased the number of pulmonary neuroendocrine cells. Future studies are needed to determine if the increase in neuroendocrine cells is causally related to changes in pulmonary function.